Suppression of angiogenesis during diabetes is a recognized phenomenon but is less appreciated within the context of diabetic retinopathy. The current study has investigated regulation of retinal angiogenesis by diabetic serum and determined if advanced glycation end products (AGEs) could modulate this response, possibly via AGE-receptor interactions. A… CONTINUE READING

FIG. 7. AGEs increase retinal ischemia and reduce neovascularization in an in vivo model. A: The hyperoxiainduced retinopathy model results in retinal ischemia (*) at P20, which drives a neovascular response depicted by hyperfluorescent preretinal fronds (arrow). B: When wild-type mice are infused with GA-MSA between P12 and P20, the retinal microvasculature shows more ischemia when compared with native-MSA controls assessed at P20, and there was a significant increase in the area of ischemia (*) in the inner retina but less neovascularization (arrow) when compared with native MSA controls. C: Gal3 / mice infused with GA-MSA fail to show the extensive ischemia evident in the wild-type mice exposed to this modified albumin. D: Quantification of retinal ischemia in wild-type mice shows that GA-MSA (f) induces enlarged areas of ischemia (indicative of suppressed intraretinal angiogenesis) at P20 when compared with native MSA controls ( ). In gal3 / mice, there is no difference between MSA control and GA-MSA treatment. For all experiments, there were a minimum of 10 mice per group, and data are presented as means SD. **P < 0.01 between GA-MSA and native-MSA treatments. E: In wild-type mice, exposure to GA-MSA causes a significant suppression of preretinal neovascularization. The gal3 / neonatal mice show a greater overall angiogenic response, and exposure to GA-MSA fails to alter preretinal neovascularization when compared with wild-type. For all experiments, there were a minimum of 10 mice per group, and data are presented as means SD. **P < 0.01 and ***P < 0.001 between GA-MSA and native-MSA treatments; #P < 0.05 between wild-type and gal3 / .